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目的探讨维吾尔族冠心病血管紧张素转换酶(ACE)基因的多态性分布及多种危险因素与冠心病(CAD)的关系。方法采用两次聚合酶链反应(PCR)方法检测152例维吾尔族包括对照组81例,冠心病组71例,测定各组ACE基因插入/缺失(I/D)多态性,并用微量比色法测定其血清ACE水平。结果与对照组比较,冠心病组DD基因型频率及D等位基因频率高于正常组,但无显著性差异(χ2=2.22,P>0.05)。血清ACE水平冠心病组ID型最高,II型最低,与正常对照组比较无显著性差异(P>0.05)。以性别、年龄、血压、体重指数、血脂指标、ACE水平、瘦素及ACE基因型为变量,行Logistic回归分析冠心病的独立危险因素,显示维吾尔族年龄(OR=1.04)、性别(OR=0.31)、ACE水平(0R=1.05)与冠心病呈正相关;而与血压、体重指数、血脂指标和瘦素水平无关,同时本研究选取的各种基因型均未进入模型。结论ACE基因I/D多态性与维吾尔族人群冠心病的发生无关,DD基因型亦不是维吾尔族冠心病的一个独立危险因素,在CAD的发病中,环境因素可能更重要。
Objective To investigate the distribution of angiotensin converting enzyme (ACE) gene polymorphism and the relationship between multiple risk factors and coronary heart disease (CAD) in Uighur coronary heart disease. Methods Two hundred and fifty Uyghur subjects including 81 controls and 71 patients with coronary heart disease were enrolled in the study. Polymerase chain reaction (PCR) was used to detect ACE gene insertion / deletion (I / D) polymorphism in each group. Determination of serum ACE levels. Results Compared with the control group, the frequencies of DD genotype and D allele in CHD group were higher than those in control group (χ2 = 2.22, P> 0.05). The level of serum ACE in coronary heart disease group was the highest, the lowest in type II, there was no significant difference compared with the normal control group (P> 0.05). Logistic regression analysis was used to analyze the independent risk factors of coronary heart disease by sex, age, blood pressure, body mass index, blood lipid index, ACE level, leptin and ACE genotype. The results showed that the Uygur age (OR = 1.04) 0.31), ACE level (0R = 1.05) was positively correlated with coronary heart disease, but not with blood pressure, body mass index, blood lipid index and leptin level, and all genotypes of this study did not enter the model. Conclusion ACE gene I / D polymorphism has no relation with the occurrence of coronary heart disease in Uighur population. DD genotype is not an independent risk factor for Uighur coronary heart disease. Environmental factors may be more important in the pathogenesis of CAD.